Klin Padiatr 2018; 230(03): 171
DOI: 10.1055/s-0038-1645009
Top 5 Cell biology and mechanisms of disease
Georg Thieme Verlag KG Stuttgart · New York

Defining the role of Id2 in human erythropoiesis

A Müller
1   Division of Pediatric Hematology and Oncology, Department of Pediatrics and Adolescent Medicine, University Medical Center of Freiburg, Freiburg, Germany
,
S Afreen
1   Division of Pediatric Hematology and Oncology, Department of Pediatrics and Adolescent Medicine, University Medical Center of Freiburg, Freiburg, Germany
,
S Bohler
1   Division of Pediatric Hematology and Oncology, Department of Pediatrics and Adolescent Medicine, University Medical Center of Freiburg, Freiburg, Germany
,
M Rizzi
2   Center for Chronic Immunodeficiency, Medical Center, Faculty of Medicine, University of Freiburg, Freiburg, Germany
,
K Schachtrup
2   Center for Chronic Immunodeficiency, Medical Center, Faculty of Medicine, University of Freiburg, Freiburg, Germany
,
M Erlacher
1   Division of Pediatric Hematology and Oncology, Department of Pediatrics and Adolescent Medicine, University Medical Center of Freiburg, Freiburg, Germany
› Author Affiliations
Further Information

Publication History

Publication Date:
08 May 2018 (online)

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    Id proteins are key regulators of differentiation and proliferation of human hematopoietic cells. They function as inhibitors of E proteins and other transcription factors. A critical factor for differentiation of hematopoietic stem cells to erythrocytes is Id2. However, recent research showed controversial results on whether Id2 acts as an inhibitor (Kim et al., 2014) or enhancer (Ji et al., 2008) of human erythropoiesis.

    We aimed at better defining the role of Id2 during different stages of human erythropoiesis. By using colony forming and human erythroid massive amplification assays of lentivirally transduced cord blood-derived CD34+ cells, we found strong evidence that Id2 constantly inhibits human erythropoiesis. Moreover, we could show that especially early stages of erythroid development are affected when Id2 is overexpressed. Prospectively, we aim at identifying specific targets of Id2 in early erythroid differentiation with focus on transcription factor binding and chromatin accessibility.


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